Highlights of the 95th Annual Meeting of the American Psychopathological Association: Prevention of Mental Illness

March 3-5, 2005; New York, NY

Joshua Fogel, PhD

Disclosures

April 20, 2005

In This Article

Cannabis Use and Schizophrenia

Robin M. Murray, MD, DSc, FRCP, FRCPsych, FMedSci, of the Institute of Psychiatry at the Maudsley Hospital, spoke about the role of environmental factors, including drug abuse, in causing schizophrenia.[7] The Aetiology and Ethnicity of Schizophrenia and Other Psychoses (AESOP) study is an epidemiologic study of all individuals aged 16 to 65 years with a first-episode psychosis in Southeast London, Nottingham, and Bristol. Data were collected between 1997 and 2000.[8] Using a structured survey, all individuals were interviewed and consensus diagnoses were made. A total of 592 individuals met the study criteria. They had matched controls (n = 400) from a random community sample of individuals each located on the same street as an individual study subject.

AESOP study results indicated different incidence rates per 100,000 individuals, depending on the city location. Southeast London had the highest incidence rates of 55 for all cases of psychoses and 42 for schizophrenia. Both Nottingham and Bristol had similar rates of 25 for all cases of psychoses and 17 for schizophrenia. Dr. Murray suggested 2 possible reasons for the higher incidence rates in Southeast London: (1) migration, as many individuals residing in that area were not born in the United Kingdom; and (2) greater rate of cannabis consumption in that area.

Per Dr. Murray, individuals with psychotic symptoms use 2 to 3 times as much cannabis as the general population. There is, however, a question of cause vs effect: that is, does cannabis use increase the risk of psychosis or do those with psychosis choose to use cannabis in order to reduce the impact of their psychotic symptoms?

Dr. Murray quoted prior research supporting the concept that cannabis use is a cause for schizophrenia. In one study of Swedish army recruits followed over 15 years, high consumers of cannabis were 6 times as likely as noncannabis users to develop schizophrenia. This included analyses adjusting for other psychiatric illnesses and social background.[9] Also, in a recently published study of a birth cohort of children followed over 25 years, daily users of cannabis had 1.6 to 1.8 times the rates of psychotic symptoms compared with nonusers.[10] In another study, those who were cannabis users by age 18 years were 1.65 times as likely to have schizophrenia by age 26 years.[11] If they used cannabis by age 15 years, they were 4.5 times as likely to develop schizophrenia by age 26 years.

On the other hand, a first look at data from the Dunedin Birth Cohort Study suggests that the cause-effect relationship may be the opposite. This data set included 1037 children assessed 10 times starting from the age of 3 years. Those who had quasi-psychotic symptoms at age 11 years were more likely to use cannabis at age 15 years. However, when Dr. Murray adjusted for these quasi-psychotic symptoms, there was still a much higher risk of schizophrenia if one had used cannabis, with an odds ratio of 3.1. He concluded that cannabis use is a risk factor for schizophrenia.

Dr. Murray also discussed the relationship of genotype to cannabis use and the risk for psychosis. Some studies show that the catechol-O-methyltransferase (COMT) genotype with the val allele confers a somewhat greater risk for schizophrenia.[12,13] In fact, researchers have found that adolescent cannabis use and the risk for schizophreniform disorder differed by COMT genotype. In their statistical analyses, those with met-met were the reference group. Among those with met-val , there was a 2.5 odds ratio; and among those with val-val, there was a greater than 10-fold odds ratio for development of schizophrenia. This all suggests that there is a genetic component for the increased risk for schizophrenia in cannabis users and otherwise.

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